A DESCRIPTIVE COMPARISON OF RESPONSE OF ORAL HYPOGLYCEMIC AGENTS AMONG T2DM IN A BACKDROP OF INSULIN RESISTANCE
Introduction:Different homeostatic models for the assessment of beta cell function in patients with insulin resistance in type 2 diabetes mellitus suggest that Dipeptidyl Peptidase (DPP-4) inhibitors cause less beta cell stress. Aims: The present study aimed to compare and contrast insulin resistance in two groups of patients taking oral hypoglycemic agents, DPP-4 plus metformin and glimepiride plus metformin, on the basis of fasting and postprandial c-peptide and insulin resistance estimated by homeostatic model assessment of insulin resistance (HOMA-IR). Methods: This preliminary descriptive observational study was conducted from 2018 to 2019 in the service Laboratory of the Department of Biochemistry, in collaboration with the Endocrinology Department, Nil Ratan Sircar Medical College and Hospital, Kolkata. Serum C-peptide, serum insulin, and plasma glucose levels were measured in both fasting and post-prandial states along with glycated hemoglobin. Result: In the fasting and fed state, the secretagogue effect of glimepiride-metformin combination was significantly higher (p = 0.017) than that of the linagliptin-metformin combination. Conclusion: Patients treated with glimepiride showed high post prandial insulin levels and high post prandial glucose excursion. This finding can be explained by the probable increase in insulin resistance, which is reflected in their post-prandial C peptide level. However, in the case of linagliptin, one mechanism of decreased post-prandial glucose is believed to be the inhibition of α-cell glucagon release, thereby relieving β-cell stress
Bargnoux, A.-S., Barrot, A., Fesler, P., Kuster, N., Badiou, S., Dupuy, A.-M., Ribstein, J., &Cristol, J.-P. (2014). Evaluation of five immunoturbidimetric assays for urinary albumin quantification and their impact on albuminuria categorization. Clinical Biochemistry, 47(16–17), 250–253. https://doi.org/10.1016/j.clinbiochem.2014.07.014
Clark, P. M. (1999). Assays for Insulin, Proinsulin(S) and C-Peptide. Annals of Clinical Biochemistry: International Journal of Laboratory Medicine, 36(5), 541–564. https://doi.org/10.1177/000456329903600501
Deacon, C. F. (2020). Dipeptidyl peptidase 4 inhibitors in the treatment of type 2 diabetes mellitus. Nature Reviews Endocrinology, 16(11), 642–653. https://doi.org/10.1038/s41574-020-0399-8
Del Prato, S., Barnett, A. H., Huisman, H., Neubacher, D., Woerle, H.-J., & Dugi, K. A. (2011). Effect of linagliptin monotherapy on glycaemic control and markers of β-cell function in patients with inadequately controlled type 2 diabetes: a randomized controlled trial. Diabetes, Obesity and Metabolism, 13(3), 258–267. https://doi.org/10.1111/j.1463-1326.2010.01350.x
Foretz, M., Guigas, B., & Viollet, B. (2019). Understanding the glucoregulatory mechanisms of metformin in type 2 diabetes mellitus. Nature Reviews Endocrinology, 15(10), 569–589. https://doi.org/10.1038/s41574-019-0242-2
Forst, T., Anastassiadis, E., Diessel, S., Löffler, A., &Pfützner, A. (2014). Effect of linagliptin compared with glimepiride on postprandial glucose metabolism, islet cell function and vascular function parameters in patients with type 2 diabetes mellitus receiving ongoing metformin treatment. Diabetes/Metabolism Research and Reviews, 30(7), 582–589. https://doi.org/10.1002/dmrr.2525
Fu, Z., Gilbert, E. R., & Liu, D. (2013). Regulation of insulin synthesis and secretion and pancreatic Beta-cell dysfunction in diabetes. Current Diabetes Reviews, 9(1), 25–53. https://doi.org/10.2174/1573399811309010025
Galgani, J. E., de Jonge, L., Rood, J. C., Smith, S. R., Young, A. A., &Ravussin, E. (2010). Urinary C-Peptide Excretion: A Novel Alternate Measure of Insulin Sensitivity in Physiological Conditions. Obesity, 18(9), 1852–1857. https://doi.org/10.1038/oby.2010.70
Galicia-Garcia, U., Benito-Vicente, A., Jebari, S., Larrea-Sebal, A., Siddiqi, H., Uribe, K. B., Ostolaza, H., & Martín, C. (2020). Pathophysiology of Type 2 Diabetes Mellitus. International Journal of Molecular Sciences, 21(17), 6275. https://doi.org/10.3390/ijms21176275
Geloneze, B., Vasques, A. C. J., Stabe, C. F. C., Pareja, J. C., Rosado, L. E. F. P. de L., Queiroz, E. C. de, &Tambascia, M. A. (2009). HOMA1-IR and HOMA2-IR indexes in identifying insulin resistance and metabolic syndrome: Brazilian Metabolic Syndrome Study (BRAMS). ArquivosBrasileiros de Endocrinologia&Metabologia, 53(2), 281–287. https://doi.org/10.1590/S0004-27302009000200020
Hardy, R. W., Cohn, M., & Konrad, R. J. (2000). Automated chemiluminescent assay for C-peptide. Journal of Clinical Laboratory Analysis, 14(1), 17–19. https://doi.org/10.1002/(SICI)1098-2825(2000)14:1<17::AID-JCLA4>3.0.CO;2-5
Holst, J. J. (2019). The incretin system in healthy humans: The role of GIP and GLP-1. Metabolism, 96, 46–55. https://doi.org/10.1016/j.metabol.2019.04.014
Jalleh, R. J., Wu, T., Jones, K. L., Rayner, C. K., Horowitz, M., & Marathe, C. S. (2022). Relationships of Glucose, GLP-1, and Insulin Secretion With Gastric Emptying After a 75-g Glucose Load in Type 2 Diabetes. The Journal of Clinical Endocrinology & Metabolism, 107(9), e3850–e3856. https://doi.org/10.1210/clinem/dgac330
Kaufman, F. R. (2002). Type 2 Diabetes Mellitus in Children and Youth: A New Epidemic. Journal of Pediatric Endocrinology and Metabolism, 15(Supplement). https://doi.org/10.1515/JPEM.2002.15.S2.737
Lebovitz, H. (2001). Insulin resistance: definition and consequences. Experimental and Clinical Endocrinology & Diabetes, 109(Suppl 2), S135–S148. https://doi.org/10.1055/s-2001-18576
Nauck, M. A., Quast, D. R., Wefers, J., & Pfeiffer, A. F. H. (2021). The evolving story of incretins ( GIP and GLP "1) in metabolic and cardiovascular disease: A pathophysiological update. Diabetes, Obesity and Metabolism, 23(S3), 5–29. https://doi.org/10.1111/dom.14496
Park, S. Y., Gautier, J.-F., & Chon, S. (2021). Assessment of Insulin Secretion and Insulin Resistance in Human. Diabetes & Metabolism Journal, 45(5), 641–654. https://doi.org/10.4093/dmj.2021.0220
Phillips, L. K., &Prins, J. B. (2011). Update on incretin hormones. Annals of the New York Academy of Sciences, 1243(1), E55–E74. https://doi.org/10.1111/j.1749-6632.2012.06491.x
Pradeepa, R., & Mohan, V. (2021). Epidemiology of type 2 diabetes in India. Indian Journal of Ophthalmology, 69(11), 2932. https://doi.org/10.4103/ijo.IJO_1627_21
Praveen, E., Sahoo, J., Khurana, M., Kulshreshtha, B., Khadgawat, R., Gupta, N., Dwivedi, S., Kumar, G., Prabhakaran, D., &Ammini, A. (2012). Insulin sensitivity and β-cell function in normoglycemic offspring of individuals with type 2 diabetes mellitus: Impact of line of inheritance. Indian Journal of Endocrinology and Metabolism, 16(1), 105. https://doi.org/10.4103/2230-8210.91204
Sacks, D. B. (2012). Measurement of Hemoglobin A1c. Diabetes Care, 35(12), 2674–2680. https://doi.org/10.2337/dc12-1348
Solis-Herrera, C., Triplitt, C., Garduno-Garcia, J. de J., Adams, J., DeFronzo, R. A., &Cersosimo, E. (2013). Mechanisms of Glucose Lowering of Dipeptidyl Peptidase-4 Inhibitor Sitagliptin When Used Alone or With Metformin in Type 2 Diabetes. Diabetes Care, 36(9), 2756–2762. https://doi.org/10.2337/dc12-2072
Tanaka, T., & Matsunaga, T. (2000). Fully Automated Chemiluminescence Immunoassay of Insulin Using Antibody−Protein A−Bacterial Magnetic Particle Complexes. Analytical Chemistry, 72(15), 3518–3522. https://doi.org/10.1021/ac9912505
Trinder, P. (1969). Determination of blood glucose using 4-amino phenazone as oxygen acceptor. Journal of Clinical Pathology, 22(2), 246–246. https://doi.org/10.1136/jcp.22.2.246-b
Walczewska-Szewc, K., & Nowak, W. (2021). Photo-Switchable Sulfonylureas Binding to ATP-Sensitive Potassium Channel Reveal the Mechanism of Light-Controlled Insulin Release. The Journal of Physical Chemistry B, 125(48), 13111–13121. https://doi.org/10.1021/acs.jpcb.1c07292
Wu, S., Gao, L., Cipriani, A., Huang, Y., Yang, Z., Yang, J., Yu, S., Zhang, Y., Chai, S., Zhang, Z., Sun, F., & Zhan, S. (2019). The effects of incretin"based therapies on β"cell function and insulin resistance in type 2 diabetes: A systematic review and network meta"analysis combining 360 trials. Diabetes, Obesity and Metabolism, 21(4), 975–983. https://doi.org/10.1111/dom.13613
Copyright (c) 2023 The Indonesian Journal of Public Health
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
- The authors agree to transfer the transfer copyright of the article to The Indonesian Journal of Public Health effective if and when the paper is accepted for publication.
- Authors and other parties are bound to the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License for the published articles, legal formal aspect of journal publication accessibility refers to Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA), implies that:
- Attribution ” You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.
- NonCommercial ” You may not use the material for commercial purposes.
- ShareAlike ” If you remix, transform, or build upon the material, you must distribute your contributions under the same license as the original.
